- Triad of *fever, **rash** and **eosinphilia*** and non *specific symptoms of AKI.*
[!INFO] Intrinsic muscle nerve supply
All the intrinsic muscles of the hand except the lateral two lumbricals cause supplied by the ulnar nerve.
The lateral lumbricals are supplied by the median nerve.
Brachials plexus is made up of C5 to T1 nerve roots
[!TIP] Mnemonic: Klumpkey the Monkey
monkey hangs -> C8/T1 lesion
| Klumpke's paralysis (KP) | Erb's palsy |
|---|---|
| C8 / T1 lesion | C5/C6 |
| Claw hand due to unopposed action of long flexors and extensors | Shoulder adducted, elbow extended, forearem pronated (waiters tip) |
| Can have associated Horner's Xn (C8,T1 are in close proximity to sympathetic chain). | Also winged scapula |
| Damage to one can cause damage to the other. | more common than Klumpke's |
| Seen in breech delivery. (upward traction on arm) | Shoulder dystocia |
| Loss of function of lubricals and wrist flexors | Deltoid, biceps, brachialis affected. |
| Lumbricals flex the MCP joints and extend the PIP and DIP joints; | |
| In KP, The wrist and the MCP are extended and the DIP and PIP are flexed. | |
| C8 / T1 - Medial forearm sensory loss | sensory loss in lateral forearm, lateral aspect of upper arm. |
Medial two lumbrical are supplied by the ulnar nerve;
Lateral two lumbricals are supplied by the median nerve.
In ulnar claw hand, the lesion is similar to klumpke's but limited to the lateral two fingers.
Causes of diabetes insipidus
| Central | Nephrogenic |
|---|---|
| Intracranial SOL / pituitary surgery / trauma etc | Lithium |
| Infiltrative diseases: Histiocytosis, Sarcoidosis, (but ?not amy_loidosis) | ⬆Ca, ⬇K |
| Haemochromatosis | Demecloclycline |
| DIDMOAD (ada Wolfram Syndrome) | Inherited: Common- ADH receptor mutation Rare: aquaporin 2 mutation |
In practice creatinine is used because it is an endogenous substance.
- But creatinine is secreted in small amounts by the tubules (15% is secreted). (ideal substance would be inulin)
"The GFR estimate is most commonly derived using 1 of 3 equations:
- the Cockcroft-Gault,[1] the modification of diet in renal disease (MDRD), or the ([Chronic Kidney Disease]) Epidemiology Collaboration (CKD-EPI).
- The MDRD and CKD-EPI equations estimate the GFR directly.
- Cockcroft-Gault is the older formula; the creatinine assay which was used to create it was not standardized;
- whereas the Cockcroft-Gault equation estimates creatinine clearance (CrCl).Source
- In the elderly, low muscle mass and low protein intake can falsely lower the serum creatinine level.
- "The Cockroft-Gault equation underestimates the GFR value in lean and elderly people, and overstates it in obese and hyperhydrated people". Source
- While the natural decline of GFR is factored into the equations above, overall, determining creatinine clearance using the Cockcroft-Gault formula provides more accurate results. Source
- Pauci-immune GN -Â PR3-ANCA GN, MPO-ANCA GN, and ANCA-negative GN (mostly have a nephritic presentation)
#2017GM-APR/Q08
#2017GM-APR/Q08
a | Light microscopy image showing thickened glomerular basement membranes (arrows; periodic acid-Schiff stain, 40×).
b | Immunofluorescence microscopy image showing granular staining for IgG along the capillary walls (40×).
c | Electron microscopy image showing subepithelial electron-dense deposits (black arrows) and basement membrane material between the electron-dense deposits (white arrows; 4,800×).
d | Immunofluorescence microscopy image showing staining for phospholipase A2 receptor (PLA2R) along the capillary walls (40×).
Diffuse glomerular membrane thickening with normal cellularity
Majority of cases are caused by autoantibodies directed against the phospholipase A2 receptor (PLA2R) found on podocytes.
About 1/3 have spontaneous remission. 40% go on to have CKD; proteinuria is often persistent even if there's no CKD.
Non selective protein loss; (albumin + other proteins)
- Right side to right side. Left to left.
- fibers from superior half travel superiorly (parietal lobe) , fibers from inferior half travel inferiorly (temporal lobe)
Lateral views showing the optic radiations:
[!INFO] Relevant cerebral lobes
Mnemonic: PITS ->
- Parietal lobe lesions -> inferior visual loss
- Temporal lobe lesions -> superior visual loss.
- Retrolenticular - inferior visual quadrants - In the parietal lobe
- sublenticular - superior visual quadrants - In the Temporal lobe.
| Characteristic | EDH-epidural/ extradural | SDH-subdural |
|---|---|---|
| Patient | Young, Hx of trauma | Old |
| Aetiology | Usually trauma, spontaneous is very rare | Commonest is traumatic, cerebral atrophy (old age, chronic alcohol use) is a major risk factor |
| - | Tamponade effect will control rate of bleeding (as it’s venous) | |
| Type of bleed | 80% arterial, therefore rapid | Mostly venous / small arteries |
| Site | Commonly middle meningeal artery at [[foramen spinosum.png]] | Bridging vein or other sites |
| Plane | Potential space between dura and skull | Between dura and arachnoid |
| Presentation | Lucid interval → rapid decrease | Can be acute or chronic. |
| Imaging | Lens shaped, does not cross suture lines, crosses dural attachments | Crescent shaped, crosses suture lines, does not cross dural attachments |
| - | Chronic changes occur: Encapsulation and resorption / hygroma formation | |
| Also seen in trauma | most common type seen in trauma | |
| Lower impact, lucid interval present | Caused by Higher energy impacts - patient won't regain consciousness | |
| brief, linear contact force to the skull. | Can Occur in less severe trauma (antigoagulants, old age are RF) | |
| Arterial or venous. (commonest site = middle meningeal artery); caused by disruption of vessels secondary to dura separating from skull. |
Mechanism: tearing of veins due to relative movement of brain due to acceleration | |
| rare in age > 60 as 'dura is tightly adherent to the skull' | highest incidence in 40s to 70s. | |
| most are acute. | Can be acute or chronic | |
| Source |
OR
Wernicke = Word Salad. (W - W)
| Wernicke's | Brocas | Conduction aphasia | Global aphasia |
|---|---|---|---|
| Receptive | Expressive | ||
| Fluent | Non fluent | ||
| "Word salad" | "Tip of the tongue" | Speech fluent; repetition poor; comprehension preserved. |
All of the above; can communicate with guestures |
| Superior temporal gyrus | Inferior frontal gyrus | Arcuate fasciculus | All regions affected |
| Middle Cerebral artery | Middle cerebral artery |
[!TIP] Mnemonic: The parietal lobe is responsible for interpretation of "things in space";
Symbols lose meaning - agraphia, acalculia, alexia,
Disorientation
Spatial structure of tactile stimuli is lost - "cortical sensory loss"
Astereognosis
[!TIP] Mnemonic:
The temporal lobe seems to be involved in
- processing and interpretation of sensory stimuli
- predominantly auditory, also visual, smell etc.
- Emotional regulation
- Memory
Functions:
Features of temporal lobe dysfunction:
| Function | Dysfunction |
|---|---|
| facial recognition | prosopagnosia - inability to identify faces |
| Language comprehension | Wernicke aphasia |
| Processing visual stimuli | Visual agnosia |
| Processing sound | Sensoryneural hearing loss, word deafness, difficulty in interpreting sounds |
| Attention | problems paying attention amidst other stimuli <-? difficulty in filtering out sensory stimuli? |
| Disrupted sensory processing during TLE | Temporal lobe epilepsy: not significant motor component as TL isn't involved in motor function. Features include déjà vu, unprovoked fear, visual distortions, and strange tastes and smells. |
| Memory | Inability to form new long term memories or if severe, loss of previous long term memories associated with self identity -> which can lead to personality change |
| Source |
Sjogren's syndrome is a cause of distal tubular acisosis.
Dysfunction of all functions of the proximal tubule.
Causes are inherited or acquired.
Inherited causes include many metabolic diseaes (cystinosis, tysosinaemia).
Causes amino acid uria, glycosuria, bicarbonateuria, phosphaturia.
| IgA nephropathy
(Berger disease) | Henoch-Schonlein (IgA vasculitis) | Goodpasture Xn | ANCA positive vasculitis |
Pathergy is a feature.
[!INFO] Pathergy:
Pathergy is an exaggerated skin injury occurring after minor trauma such as bump, bruise, needle stick injury. A more severe injury, such as a surgical procedure, can result in persistent ulceration in a patient with pathergy. It typically occurs in patients with Behcet disease.
Pathergy occurs in :
- Sweet syndrome
- Behcet-disease
- Pyoderma ganrenosum
DD for neutrophillic dermatosi: Sweet syndrome
Biopsy: INTENSE neutrophilic infiltrate with no evidence of infection or vasculitis.
#2017GM-APR/Q10
Treatment: steroids and immunosuppresants.
Sweet syndrome:
Causes of QT prolongation:
| Congenital | Drugs | Other |
|---|---|---|
| - Jervell-Lange-Nielsen syndrome (includes deafness and is due to an abnormal potassium channel) - Romano-Ward syndrome (no deafness) |
- amiodarone, sotalol, class 1a antiarrhythmic drugs - tricyclic antidepressants, fluoxetine - chloroquine - terfenadine - erythromycin |
- electrolyte: hypocalcaemia, hypokalaemia, hypomagnesaemia - acute myocardial infarction - myocarditis - hypothermia - subarachnoid haemorrhage |
The classic description of the left cardiac ventricle is as containing two papillary muscles: the anterolateral and posteromedial.[2] The anterolateral arises from the sternocostal wall, and the posteromedial papillary muscle arises from the diaphragmatic wall of the ventricle. The right ventricle contains three papillary muscles, classically described as anterior, posterior, and septal. Source
Left anterolateral papillary muscles derives from branches of the left coronary artery. The blood supply to the left posteromedial papillary muscles most commonly derives from the right coronary artery Source
The eosinophil is the most characteristic cell that accumulates in asthma and allergic inflammation. Activated eosinophils produce lipid mediators, such as leukotrienes and platelet activating factor, that mediate smooth muscle contraction - UpToDate.
[!INFO] Azithromycin
used as last resort add on therapy
Reduces exacerbation frequency but promotes antibiotic resistance.
#2017GM-APR/Q09
Some people can get asthma without atopy.
i.e excercise induced asthma, cold induced asthma, stress, anxiety. etc.
Pathologic findings in pulmonary arterial hypertension:
Treatment:
Two groups:
Disease modifying drugs in rheumatoid arthritis;
DMARDS are commonly co-prescribed;
Are there any bad combinations?
The drugs are divided into non-biologics and biologics, corticosteroids, and NSAIDS.
Usuallly RA doesn't have adverse effects on pregnancy.
TNF is central in disease pathogenesis.
Order of preference for use of drugs:
[!INFO] Key terms:
- Reverse transcription -> using RNA to produce DNA.
- Retrovirus -> A RNA virus which uses reverse transcription to produce DNA which is then incorporated into host DNA
Examples:
Hepatitis B - hepadnaviridae
Hepatitis C - flaviviridae
HIV - retroviridae
EBV - herpesviridae
picornaviruses include - enterovirus, coxsackie virus, Hepatitis A
Orthomyxoviridae - influenza virus.
Retroviruses - HTLV-1 and HIV. (HIV uses viral integrase for DNA incorporation)
Source
Antiviral drugs do no "kill" viruses; they only inhibit replication.
[!INFO] Summary
New herpes is bad; worst if onset in T3.
Recurrence of herpes doesn't impose a significant risk.
ADH stimulates V2 rectors on principal cells in the collecting duct to promote insertion of aquaporin channels.
The main cells in the collecting duct are principal cells. They
The intercalated cells are responsible for H+ secretion and chloride secretion.
| Chloride responsive | Chloride resistant |
|---|---|
| GI H+ loss | HCO3- retention |
| contraction alkalosis | Intracellular H+ shift |
| Diuretic therapy | Hyperaldosteronism |
| Post hypercapnia | Barter syndrome |
| Cystic fibrosis | Gitelman syndrome |
| Exogenous alkalotic | |
[!INFO] Pendrin
Is a key transport protein involved in pathogenesis.
The transcellular shifts in K+ caused by acid base changes.
Basis: In acidosis, about half the H+ is buffered intracellularly. To maintain electroneutrality, intracellular K+ moves outwards into the ECF.
[!INFO] Hypoaldosteronism
In patients with hypoaldosteronism, for example, the mild metabolic acidosis is primarily due to the associated hyperkalemia
UpToDate
Causes of gynaecomastia
| Group | Cause | Mechanism |
|---|---|---|
| Physiologic | newborns | |
| Puberty | ||
| Old age | ||
| Pathologic |
Drugs | |
| Cirrhosis or malnutrition | ||
| Male hypogonadism - primary or secondary | ||
| Tumors | ||
| Testicular - germ cell, Leydig cell, Sertoli cell, sex cord | ||
| Adrenal - adenoma or carcinoma | ||
| Ectopic production of human chorionic gonadotropin | ||
| Hyperthyroidism | ||
| Chronic kidney disease and dialysis | ||
| Rare causes | ||
| Enzymatic defects of testosterone production* | ||
| Androgen-insensitivity syndromes* | ||
| True hermaphroditism* | ||
| Aromatase excess syndrome |
[!TIP] mnemonic: Drugs causing gynaecomastia
Gay DISCO
- Goserelin - Mechanism of Action Goserelin (a gonadotropin-releasing hormone [GnRH] analog) causes an initial increase in luteinizing hormone (LH) and follicle stimulating hormone (FSH), chronic administration of goserelin results in a sustained suppression of pituitary gonadotropins
- Digoxin
- Isoniazide
- Spironolactone
- Cimetidine
- Oestrogen
#2023GM-NOV/Q30
See also [[Hormone Physiology#Prolactin]]
Pathological causes
Drugs:
A rare #autosomal-Recessive disorder which presents with
Unilateral:
| Painful | Painless |
|---|---|
| Corneal abrasion | Lens dislocation |
| Keratitis | Vitreous haemorrhage |
| Acute Glaucoma | Acute maculopathy |
| Hyphema | Retinal detachment |
| Endophthalmitis | Retinal artery occlusion |
| Anterior Uveitis | Retinal Vein occlusion |
| Optic Neuritis | Ischemic optic neuropathy |
Bilateral
[!INFO] Visual loss means loss of one or more of
- acuity
- Color vision
- visual field
Central Vs. Peripheral vision loss:
Speed of onset
| Retinal artery occlusion (RAO) | Retinal Venous occlusion (RVO) |
|---|---|
| Less common | Much more common |
| Older population | older population |
| Urgent need of further evaluation | Doesn't need further evaluation for cause |
| Higher risk of ASCVD events | |
| Managed by neurologist - like a stroke | Managed by ophthalmologist |
| Permanent renal death in a few hours. | |
| Commonest causes are emboli: + ICA emobli + aortic arch, cardiac |
|
| Sudden vision loss (curtain coming down) | Vision loss ranges from slight to severe |
| Retinal haemorrhages are common | |
| Vascular causes are the main risk factors | Age seems to be the main risk factor |
| Source |
#autosomalDominant
Hallmarks:
retinal and central nervous system (CNS) hemangioblastomas (blood vessel tumors), pheochromocytomas, multiple cysts in the pancreas and kidneys, and an increased risk for malignant transformation of renal cysts into renal cell carcinoma.
Source
#autosomalDominant
| Gastric polyps | mucocutaneous pigmentation |
[!TIP] Summary
Small anterior pituitary tumours (<1cm) are commmon, nonfunctioning and asymptomatic.Large pituitary tumours (>1cm) are less common and they can cause pressure effects or hormone imbalances.
In contrast to macroadenomas, pituitary function testing is generally not needed for microadenomas - Medscape
Pituitary microadenoma is usually an incidental finding on MRI head. Patients are asymptomatic unless the tumor is hormonally active.
Pituitary macroadenoma presents with mass effects and potentially hormonal deficiency or hormonal excess. Source
[!TIP] Summary:
Mobitz I : OK
Mobitz II : BAD
Management: intravenous alpha1-antitrypsin protein concentrates + smoking cessation, supportive bronchodilators etc .
Source <- Dynamic air trapping in COPD.